Pregnancy and Dystocia
World Small Animal Veterinary Association World Congress Proceedings, 2013
Philip Thomas, BVSc, PhD, FACVSc, DACT
Queensland Veterinary Specialists, Stafford Heights, Queensland, Australia


Pregnancy is supported by luteal progesterone, in turn supported by pituitary LH and prolactin. Prostaglandins and dopaminergic agents are luteolytic. Hematologic and biochemical changes occur (Table 1) and definitive indicators of pregnancy are listed (Table 2). Days are from LH peak. Embryos (8–16 cells) are present from 10 d in the oviduct; morulae with zona pellucid are in uterine horns at 12 d; and blastocysts migrate between horns 13–14 d. Migration stops d 17. Pregnancy-associated anorexia (50%) and vomiting (25%) have recently been described (Taylor, Thomas 2012).

Table 1. Pregnancy physiologic changes


Pregnancy-associated change


Falls from day 28 to 40% (d 35) and < 35% (d 63)

Body weight

Increases 20–50% in second half of pregnancy


Falls in second half of pregnancy


Falls to < 500 mg/dl after d 21


Peaks at d 30 then falls and peaks again at parturition



Acute-phase proteins

Increase in first trimester


Decreases in response to rising progesterone


Reduced sensitivity to insulin after d 35



Total protein



Falls in last trimester




Rises from d 20


Rises from preceding estrus


Peak in proestrus and late pregnancy

Growth hormone*



Rises from d 35

* Parameters also change in diestrus.

Table 2. Indicators of pregnancy in the bitch and queen





Vesicles palpable d 21
Poor sensitivity and specificity

Vesicles palpable d 21


Fetal skeletons d 45
Good sensitivity and specificity
Litter size/fetal size?
Fetal death of > 24 hours detectable

Fetal skeletons d 38


Vesicles detected d 20
Fetal heart rates, litter size d 25–28
Viability, uterine disease detectable

Vesicles detected d 17

Acute-phase proteins

Fibrinogen, haptoglobin, C-reactive protein
Peak d 20–30; false + common



Detectable d 20; in-clinic assay; false + and -


Early Embryonic Death and Abortion


Reliable data not available, up to 25% of conceptions may not result in birth. Bacterial infection is over-diagnosed when specific infectious causes are limited to Brucella canis and herpesvirus canis in the bitch.


Fetal defects; maternal environment (cardiac disease, reduced uterine blood flow, uterine disease, progesterone-associated, diabetes mellitus, drugs (Table 3); trauma; infection (Brucella canis and other Brucella spp., herpesvirus canis, Minute Virus of Canines, Bluetongue virus, Campylobacter jejuni, Salmonella spp., Listeria monocytogenes, Escherichia coli, opportunistic bacteria, Toxoplasma gondii, Mycoplasma spp., Ureaplasma spp.).


Poorly documented except in the case of B. canis where bacterial infection causes placentitis.

Clinical Presentation

Early loss unnoticed; vaginal discharge with loss in the last half of pregnancy; occasionally fetal expulsion with late abortion.


Difficult and unrewarding. Steps include: history including potential teratogens and changes to the environment; systemic/reproduction exam; hematology, biochemistry, and urinalysis; imaging; culture of vaginal discharge and abortus; histology.


Supportive therapy and symptomatic treatment of the dam, which might include intravenous colloids and antibiotics if systemic disease is present. Rarely, pregnancy can continue if viable fetuses are present. If viable fetuses are not present, uterine contents may be expelled by the dam or may require expulsion with ecbolic agents or by ovariohysterectomy.

Table 3. Drugs and chemicals shown to cause pregnancy-associated disease or
teratogenicity in the bitch/queen/woman. Particularly avoid organogenesis, day 11–34

Heavy metals

Lead, mercury


Of any kind, at adequate dosage


Tetracyclines, streptomycin, nitrofurantoin, chloramphenicol, griseofulvin, ketoconazole


Carbaryl, diazinon, dichlorvos


Progestins, estrogens, androgens, anabolics


Primidone, phenobarbitone, cimetidine, antiprostaglandins, prolactin antagonists



A manifestation of normal physiology, all bitches are pseudopregnant (overt or covert) following estrus.


Overt signs occur at the end of diestrus when progesterone falls and prolactin rises.

Clinical Presentation

Females might show no clinical signs or show mammary gland development, abdominal enlargement, weight gain, and changes in behavior.

Differential Diagnosis



Physical findings, history, imaging


Most require no treatment. Reduce food and water intake with care. Avoid phenothiazines (e.g., acetylpromazine), which inhibit dopamine and promote prolactin secretion. Bromocriptine (20–30 µg/kg PO q 24 h) or cabergoline (5 µg/kg PO q 24 h) will inhibit prolactin. Treatment with progestogens will resolve signs; however, when progestogens discontinued, clinical signs recur.

Uterine Torsion


Uncommon life-threatening condition in a near-term pregnancy


The gravid uterus rotates about its long axis from the focus of the uterine body (both horns) or base of one uterine horn (single horn).

Clinical Presentation

Acute-onset abdominal pain, tenesmus, serosanguineous vaginal discharge; plus dystocia if at term

Differential Diagnosis

Any systemic disease of late pregnancy


Imaging and clinical findings


Surgical correction of the torsion and delivery of the neonates are indicated. Partial or complete hysterectomy if ischemia has caused necrosis.

Uterine Rupture


A rare prepartum or intrapartum event


Associated with abdominal trauma in the last trimester, obstructive dystocia, or following administration of uterine ecbolic agents.

Clinical Presentation

Acute abdomen in a peri-parturient bitch. Free-floating mummified fetuses have been reported as incidental finding.


Exploratory laparotomy

Acromegaly and Diabetes Mellitus


Progesterone is an agonist of growth hormone (GH) and an antagonist of insulin. Therefore, acromegaly and diabetes mellitus can occur in diestrus and pregnancy.


Acromegaly is caused by an excess secretion of GH leading to overgrowth of soft and bony tissue, caused by either exogenous progestogens used to prevent estrus or endogenous progesterone during diestrus. Excess GH also results in hyperglycemia, carbohydrate intolerance, and, eventually, insulin-resistant diabetes mellitus.


Increased progesterone concentrations during diestrus or pregnancy stimulate excess secretion of GH, which may inhibit postreceptor pathways or cause downregulation of insulin receptors in some animals, leading to diabetes mellitus.

Clinical Presentation

Acromegaly: Interdental spaces are increased and there is usually excessive skin and wrinkling in combination with edema, particularly of the limbs, throat, and head. Animals with advanced disease may present with a hoarse voice as a result of the pharyngeal tissue hyperplasia.


The conditions are transient and usually resolve once the source has been controlled.

Eutocia and Dystocia

Normal Pregnancy Length and Parturition

Length is affected by breed and litter size, but not age or parity (Eilts 2005). Parturition date can be predicted from estrus progesterone data, pregnancy fetal sonography (biparietal diameter and body diameter, Stanczyk et al. 2012), and terminal rectal temperature monitoring. Parturition can be induced (Ram Chandra Reddy et al. 2012).

Table 4. Length of pregnancy

58 to 72 d

From any breeding date

64 to 66 d

From the LH peak or progesterone rise > 6–8 nmol/L

56 to 58 d

From the first day of cytologic diestrus

Stage I labor 6–12 h: Begins with uterine contractions of reducing interval, ends with cervical dilatation; bitch restless, nervous, pants, paces, vomits, shivers.

Stage II (SII, fetal delivery) and III (placental delivery) labor 0–18 h: Begins with abdominal contractions and/or fetal fluid expulsion and/or pup birth; pup born at least every two hours; placenta delivered 0–15 minutes after pup, maybe after all pups; delivery alternates between uterine horns; posterior presentation in 40% of pups.

Table 5. Indicators of impending parturition

Time prepartum

0–7 d

Behavioral change

12–24 h

Nesting intensifies

0–14 d


10–24 h

0.5–1.0°C drop in rectal temperature

0–24 h

Progesterone < 6–8 nmol/L

0–12 h

Fetal heart rates < 180 bpm

Table 6. Indicators for examination/intervention

> 72 d

From any breeding

> 66 d

From LH peak

> 60 d

From day 1 of diestrus

> 24 h

From fall in rectal temperature and/or progesterone < 6–8 nmol/L

> 2 h

From onset of Stage II labor to pup; or between pups

> 2 h

From onset of green or black or bloody vaginal discharge

> 20 min

Active continuous abdominal contractions

> 20 min

From pup presentation at vulva to birth


Fetal heart rates < 180 bpm


Obstruction to birth canal


Bitch weak, sick, painful


Dystocia is an inability of the bitch to complete eutocia (normal vaginal delivery). Dystocia can be categorized by presentation and subcategorized into aetiology.


Failure to begin Stage I or II/prolonged active Stage II/cessation of Stage II

Aetiology: Maternal Origin

 Systemic: primiparous, > 6 yo, toy breed, brachycephalic

 Abdominal: age > 6 y, abdominal hernia, diaphragmatic damage

 Pelvis: immature, fracture, neoplasia, degeneration, developmental anomaly, breed, fat

 Uterus: trauma, rupture, torsion, developmental anomaly

 Endocrine: abnormal estrogen, progesterone, thyroid function, relaxin, prolactin, PGs, oxytocin, other?

 Metabolic: abnormal calcium, glucose, other electrolyte

 Myometrial: singleton, age, overstretching (large litter)

 Cervix, vagina, vulva: immature, insufficient dilatation, fibrosis, disease, neoplasia, developmental anomaly


Aetiology: Foetal Origin

 Fetal oversize: breed, small litter size

 Developmental anomaly (e.g., anasarca)

 Fetal position: ventral (dorsopubic), lateral (dorsolateral)

 Fetal posture posterior: hock flexion, hip flexion

 Fetal posture anterior: head flexion, shoulder/elbow flexion

 Fetal presentation: transverse/bicornual, simultaneous

 Fetal abnormality: breed-associated, random, fetal death (?)


Physical and reproduction examination, digital rectal, abdominal palpation, vaginal cytology, hematology, biochemistry, blood gas and electrolytes, imaging.


Deliver any pup in the birth canal; diagnostic workup; correct any fluid, electrolyte, calcium, and glucose imbalances. Caesarian section is indicated if medical management will not result in timely delivery of live pups. Uterine ecbolics are indicated in special circumstances only. Oxytocin is misused, with excess causing tetanic and unproductive uterine contractions, placental separation and fetal hypoxia. Oxytocin stimulates smooth muscle contraction by increasing sodium permeability of uterine myofibrils. Oxytocin affects the rate of influx of calcium into myometrial cells and requires adequate extracellular calcium concentration. Oxytocin is contraindicated for obstructive dystocia, closed cervix, fetal distress, systemic bitch illness, placental separation, uterine disease, and uterine rupture. Wheaten's (1989) data support the use of oxytocin only at 1–5 IU SC or IM giving 20-min duration. Repeated use is controversial. Published success rates are modest (Darvelid, Linde-Foresberg 1994). Tocodynamometry has been proposed to provide objective measurement of uterine contractions (by measuring intrauterine and intraamniotic pressure) to prevent the use of oxytocin in the presence of normal or hypertonic contractions (Copley 2001). Fetal viability can be assessed with APGAR scoring and umbilical lactate as a measure of fetal acidosis (Groppetta et al. 2010).

Caesarian Section

Real data are scant. Ayers and Thomas (2010) revealed median age 4; brachycephalic breeds overrepresented; 9% and 18% had vaginal and uterine abnormalities, respectively; modal lowest fetal HR = 160 bpm; mean litter size 5.6; and pup mortality rate = 11.5%. Aetiology was maternal 13.2%, fetal 37%, and litter size 16.5%. Acceptable outcomes follow ventral midline approach; single incision at the base of one horn and Utrecht pattern to suture hysterotomy. Repeat Caesarians result in reduced litter size of approximately one pup and are otherwise associated with no change to maternal or fetal mortality (Haysom, Thomas 2012). Propensity for caesarian may be heritable (Thomas, unpublished data).


1.  Ayres SE, Thomas PGA. Population characteristics of 453 bitches undergoing 510 caesarian section procedures between 1999 and 2009: a retrospective study. Clin Therio. 2010;2:451–465.

2.  Copley K. Canine parturition management. Soc Therio Proc Ann Conf Canine Symp. 2001:311–315.

3.  Darvelid AW, Linde-Forsberg C. Dystocia in the bitch, a retrospective study of 182 cases. J Small Anim Pract. 1994;35:402–407.

4.  Eilts B, Davidson AP, et al. Factors influencing gestation duration in the bitch. Theriogenology. 2002;64:242–251.

5.  Groppetti D, Pecile A, Del Carro AP, et al. Evaluation of newborn canine viability by means of umbilical vein lactate measurement, apgar score and uterine tocodynamometry. Theriogenology. 2010;74:1187–1196.

6.  Haysom L, Thomas PGA. Effect of prior caesarian on bitches presented for caesarian section. In: Proc Aust College Vet Sci Science Week, Gold Coast, Australia; 2012.

7.  Ram Chanra Reddy K, Sada Siva Rao K, Raju KGSD. Induction of whelping in bitches using dinoprost, cloprostenol and mifepristone. In: Proc 7th Inter Symp Canine Feline Reprod. Whistler, Canada; 2012.

8.  Stanczyk E, Antonczyk A, et al. Comparison of efficacy of two biometric parameters for prediction of the parturition date in second half of pregnancy in the bitch. In: Proc 7th Inter Symp Canine Feline Reprod. Whistler, Canada; 2012.

9.  Taylor S, Thomas PGA. Pregnancy associated anorexia in the bitch. In: Proc Aust College Vet Sci Science Week, Gold Coast, Australia; 2012.

10. Wheaton LG. Drugs that affect uterine motility. In: Kirk RW, ed. Current Veterinary Therapy X: Small Animal Practice. Philadelphia: WB Saunders; 1989:1299–1302.


Speaker Information
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Philip Thomas, BVSc, PhD, FACVSc, DACT
Queensland Veterinary Specialists
Stafford Heights, Queensland, Australia

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